Mathison R, Woodman R, Davison J S
Department of Physiology and Biophysics, Faculty of Medicine, The University of Calgary, AB, Canada.
Can J Physiol Pharmacol. 2001 Sep;79(9):785-92.
The role of the D-isomeric form of the salivary gland tripeptide FEG (feG) and its carboxyl-amidated derivative, feG(NH2), in regulating leukocyte adherence to nonfixed atrial slices from Sprague-Dawley rats was examined under static conditions. Optimal binding of the leukocytes was seen if the leukocytes were treated with platelet activating factor (PAF; 10(-9)M). The increased adherence of PAF-treated peripheral blood leukocytes was totally inhibited by both feG and feG(NH2) (10-9M), as well as by antibodies against CD18 and CD49d. In contrast, the binding of peritoneal leukocytes was blocked only by CD49d antibody. Circulating leukocytes obtained from lipopolysaccharide (LPS) treated (2 mg/kg ip) rats did not bind to atrial slices obtained from normal hearts, but readily bound to atrial slices obtained from LPS-treated rats. This leukocyte binding was inhibited by in vivo feG treatment (100 microg/kg ip, 24 h before harvest) or by treating the isolated cells with feG (10(-9)M). The amidated peptide feG(NH2) reduced neutrophil accumulation in the atrium elicited by ip injection of LPS, whereas feG was ineffective. The reduction in neutrophil infiltration into the myocardium by feG(NH2) and the prevention of leukocyte interaction with myocytes seen with both feG and feG(NH2) probably results in hindered leukocyte migration in the inflamed heart, resulting in less tissue damage. The inhibition by these tripeptides on neutrophil adhesion to myocytes suggests that salivary glands hormones regulate the severity of cardiac inflammation.
在静态条件下，研究了唾液腺三肽FEG（feG）的D-异构体形式及其羧基酰胺化衍生物feG(NH2)对Sprague-Dawley大鼠非固定心房切片中白细胞黏附的调节作用。如果用血小板活化因子（PAF；10(-9)M）处理白细胞，则可观察到白细胞的最佳结合。feG和feG(NH2)（10-9M）以及抗CD18和CD49d抗体完全抑制了PAF处理的外周血白细胞黏附增加。相比之下，腹膜白细胞的结合仅被CD49d抗体阻断。从脂多糖（LPS）处理（2mg/kg腹腔注射）的大鼠获得的循环白细胞不与正常心脏的心房切片结合，但容易与LPS处理的大鼠的心房切片结合。这种白细胞结合可通过体内feG处理（收获前24小时腹腔注射100μg/kg）或用feG（10(-9)M）处理分离的细胞来抑制。酰胺化肽feG(NH2)减少了腹腔注射LPS引起的心房中性粒细胞积聚，而feG则无效。feG(NH2)减少中性粒细胞浸润到心肌中，以及feG和feG(NH2)都能防止白细胞与心肌细胞相互作用，这可能导致炎症心脏中白细胞迁移受阻，从而减少组织损伤。这些三肽对中性粒细胞与心肌细胞黏附的抑制作用表明，唾液腺激素调节心脏炎症的严重程度。
